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1HOURContinuing EducationCE

Imagine a patient with a history of stroke that has affected her right side, particularly her right arm, hip, leg, and foot. She has both spasticity

and clonus, which she manages by using an intra-thecal baclofen pump—she finds the sedative effects of oral baclofen intolerable. She likes to stay active and performs regular stretches at home. (This case is a composite based on our experience.)

One day, the patient calls her clinic to report that she is experiencing muscle tightness in her left arm. The nurse relays the information to the physician, who orders an increase in the intrathecal baclofen dosage. A nurse visits the patient at home to increase her dos-age in accordance with the revised order. Within an hour, the patient is confused and lethargic. She is ad-mitted to the hospital. What went wrong?

It’s important for clinicians to bear in mind that spasticity, clonus, and muscle tightness are three dis-tinct conditions. While spasticity and clonus are neu-rogenic in nature, muscle tightness is myogenic. The effective management of these movement disorders depends in large part on the clear description of the patient’s signs and symptoms.

In this scenario, the nurse should not have as-sumed that, simply because the patient uses an intra-thecal baclofen pump, a change in her symptoms was due to spasticity. A thorough triage would have re-vealed that, though the patient’s spasticity affects her right side, she reported left-sided muscle tightness, which could have been managed conservatively with heat, ice, and additional short-term oral medication. Instead, she received an increased dosage of intrathe-cal baclofen, which resulted in an overdose, as evi-denced by her confusion, drowsiness, and lethargy.

Neuromuscular signs and symptoms occur across a multitude of diseases and injuries. For example, muscle tightness may be experienced after a fall, mo-tor vehicle accident, or sprain. Successful symptom management requires effective communication about symptoms, yet there are often discrepancies between patient and provider descriptions of neuromuscular symptoms and manifestations.1 Further complicating matters, neuromuscular signs and symptoms can exist as single entities or in clusters. For example, a person with muscle tightness may or may not experience pain and muscle weakness; clonus may or may not coexist

ABSTRACT: Neuromuscular disorders are complex, difficult both to differentiate and to manage. Yet nurses, who encounter a symptomatically diverse neuromuscular patient population in various practice settings, are expected to be well versed in managing the variable associated symptoms of these disorders. Here the au-thors discuss how to assess such neuromuscular conditions as muscle tightness, spasticity, and clonus; the pathophysiology underlying each; and the available recommended treatments, an understanding of which is necessary for successful symptom management and clear provider–patient communication.

Keywords: clonus, movement disorders, muscle tightness, neuromuscular disorders, spasticity

Recognizing crucial distinctions between muscle tightness, spasticity, and clonus.

Managing Movement Disorders: A Clinical Review

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Isotonic contractions change the length of skeletal muscles, enabling people to move objects. Isotonic contractions that shorten the muscle are called con-centric; those that lengthen the muscle are called ec-centric. Concentric contractions allow people to lift objects and eccentric contractions allow people to set them down.

Eccentric contractions commonly lead to skeletal muscle injuries. Such injuries, commonly called strains, can lead to muscle tightness. First, a hematoma forms at the site of the tear. Immune cells then infiltrate to begin the repair process, causing swelling and in-flammation but also removing the cellular debris so the injury can be repaired. Satellite cells, which are muscle-specific stem cells, proliferate, fuse into myo-tubes, and fill in the tear. Whether healing is successful depends on the severity of the strain. If many fibers and supporting connective tissues are damaged, the injury may result in prolonged pain, atrophy, muscle weakness, loss of flexibility, and disorganized replace-ment of the connective tissue.

Isometric contractions produce tension without causing the muscle to change in length, as when a person tries to move an item that’s too heavy to lift. A movement may have components of both isomet-ric and isotonic contractions, depending on what the movement requires of the muscles involved.

Assessment. There is no standardized way to as-sess muscle tightness. Evidence of muscle tightness is both objective and subjective. The most common objective means of assessment is to measure the pa-tient’s active and passive range of motion with a go-niometer, a protractor-like instrument that clinicians

By Rozina Bhimani, PhD, DNP, APRN, Frank Medina, and Lisa Carney-Anderson, PhD

with spasticity. Symptom differenti-ation and discrimination based on appropriate assessment and knowl-edge of neuromuscular pathophysi-ology is the first step in initiating a nursing care plan for a patient with a movement disorder. Since nurses working in diverse practice set-tings are likely to encounter such patients, this article discusses the pathophysiology and assessment of three different, common neuromus-cular disorders—muscle tightness, spasticity, and clonus—as well as the treatment options for each.

MUSCLE TIGHTNESSMuscle tightness may occur af-ter any acute injury that strains or tears the soft tissue. The patient of-ten experiences swelling, bruising, weakness, and the inability to fully stretch the muscle. Common acute injury sites are the back, hamstring, quadriceps, and gastrocnemius. Muscle tightness may also result from sustained pos-tures. For example, “text neck” refers to a tightness of neck muscles from prolonged texting on a cell phone.2, 3 If not properly assessed and treated, muscle strain may lead to chronic muscle tightness. Cur-rently, there is no consensus definition of muscle tightness, though the National Library of Medicine categorizes it as a form of muscle tonus.4

Pathophysiology. Skeletal muscles consist of long multinucleated cells called muscle fibers, each of which can extend the entire length of the muscle. Fascicles are bundles of muscle fibers wrapped in connective tis-sue. Skeletal muscles are composed of several fascicles wrapped in a connective tissue sheath called fascia. The connective tissue surrounding the entire muscle is continuous with the tendons that anchor the muscle to the skeleton (see Figure 1). The tendon attachment that remains fixed in place is called the origin; the ten-don attachment that moves with muscle contraction is called the insertion.

On a cellular level, skeletal muscle fibers are com-posed of the filamentous proteins actin and myosin, which are interspersed in orderly, repeated units called sarcomeres. With a muscle contraction, the shortening of many sarcomeres in a series allows the muscle fibers and ultimately the entire muscle within its layers of connective tissue to shorten. The forces generated by the sarcomeres during muscle contrac-tion are transmitted to the connective tissue around the contracting fibers by protein complexes known as costameres.

Muscle �ber (cell)

SarcomereTendon

Bone

FasciaBlood

vessels

Fascicle

Figure 1. Anatomy of a Muscle

With every muscle contraction sarcomeres shorten, causing the muscle fibers and ulti-mately the entire muscle itself to shorten. The forces generated by this contraction are transmitted to the connective tissue (fascia) that surrounds the contracting muscle fi-bers, resulting in movement. Illustrations by Sara Jarret.

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can use to quantify, in degrees, joint angle and range of motion in a patient’s limbs. However, to assess muscle tightness in other parts of the body, such as the abdomen, clinicians must rely on palpation, pa-tient history, and patient reports of pain. A patient’s subjective report is crucial in assessing muscle tight-ness. If a patient reports that muscle tightness is in-creasing, that self-report should be accepted and the tightness treated accordingly. Numeric rating scales, which are commonly used to assess many conditions, may also be used to assess muscle tightness.

Treatment. Muscle tightness is often initially treated with ice or heat. After an acute injury, it’s generally recommended that ice be used for the first 24 hours and heat later. The frequency of ice appli-cation varies with patient tolerance but applying ice in 15-to-20-minute increments is often helpful. Heat applied in 10-to-15-minute increments often relieves chronic muscle tightness, though no specific frequency is recommended. When applying heat, it’s important to ensure that patients’ sensation is intact and that the heat source is not too hot.

Muscle tightness can also be managed with a cen-trally acting muscle relaxant, such as cyclobenzaprine (Amrix) or methocarbamol (Robaxin), though these drugs are not recommended for older adults, given their anticholinergic activity and cyclobenzaprine’s long half-life.5 Since muscle tightness can entrap local nerve endings, it may produce pain and stinging sen-sations. If muscle tightness becomes chronic, it may require physical or occupational therapy, and severe chronic cases may produce contractures, requiring tendon-lengthening surgery.

SPASTICITYSpasticity, which manifests as neurogenic muscle tightness, may occur as a sequela of such neuromus-cular disorders as spinal cord injury, multiple scle-rosis, stroke, or traumatic brain injury, with reported prevalence and annual incidence varying widely. Ac-cording to a systematic review by Martin and col-leagues, the prevalence of lower limb spasticity per 100,000 is 2 to 350 in multiple sclerosis, 240 to 360 in cerebral palsy, 22 to 90 in spinal cord injury, and 40 to 600 in stroke; the annual incidence of lower

limb spasticity per 100,000 is 100 to 235 in traumatic brain injury, 30 to 485 in stroke, and 0.2 to 8 in spi-nal cord injury.6

Although researchers agree that spasticity is an upper motor neuron syndrome, there is no consensus on its definition. In 1980, Lance defined spasticity as a component of the upper motor neuron syndrome that results from “hyperexcitability of the stretch re-flex” and is characterized by a “velocity-dependent increase in tonic stretch reflexes.”7 Subsequent re-searchers have described spasticity similarly.8-11

However, in 2005, the Support Programme for Assembly of a Database for Spasticity Measurement (SPASM) proposed the following as a new definition for spasticity: “disordered sensory-motor control, re-sulting from an upper motor neurone lesion, present-ing as intermittent or sustained involuntary activation of muscles.”12 By identifying the roles played by both the nervous and musculoskeletal systems in produc-ing spasticity, this newer definition is broader in that it recognizes the role of sensory involvement in spas-ticity.

Upper motor neuron pathway disorders may pro-duce pain, insomnia, and pressure injuries, reducing quality of life and increasing caregiver burden.13 In addition, they can prevent the transmission of infor-mation essential for such vital functions as walking, breathing, and swallowing. Some degree of spasticity, however, may benefit certain patients, providing tone for weak muscles and thereby aiding in ambulation and transfer.

Pathophysiology. Spasticity stems from a disrup-tion of upper motor neuronal pathways that normally send messages from the brain to the spinal cord to exe-cute muscle functions. Impairment of the descending inhibitory pathways of the corticospinal tract results in increased excitability of the α motor neurons, which innervate skeletal muscles (see Figure 2). The increased α motor neuronal excitability, in turn, causes muscle tightness and contracture, particularly in the flexor muscles.14

Assessment. Symptoms of spasticity may be inter-mittent or sustained. Urinary tract or other infections, renal calculi, pressure injuries, constipation, poorly fit-ting orthotics, and other maladies may act as noxious

A patient’s subjective report is crucial in assessing

muscle tightness. If a patient reports that muscle

tightness is increasing, that self-report should be accepted

and the tightness treated accordingly.

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stimuli and exacerbate spasticity.15 This may be be-cause the same changes that cause an enhanced re-sponse to the stretch reflex in patients with upper motor neuron damage also increase sensitivity of the spinal cord to sensory input from painful stimuli. Al-though patients’ experience of spasticity is subjective, symptoms can be assessed using the Ashworth or Modified Ashworth scale, which relies on examiner observation.16 The use of these scales requires assess-ment expertise and close attention paid to changes in patient responsiveness over time and with intervention.

The Ashworth scale is a five-level (0 to 4) ordinal scoring scale developed in 1964 by Bryan Ashworth to evaluate the clinical efficacy of the antispasmodic medication carisoprodol in patients with multiple sclerosis.17 Scores are assigned based on the resis-tance or “catch” of patients’ limbs as clinicians guide the patients through a passive range of motion exer-cises. In 1987, to enhance the scale’s sensitivity, Bo-hannon and Smith added a level (1+) to the scale between the scores 1 and 2, creating the Modified

Ashworth scale.18 In addition to these scales, clini-cians consider patients’ rating of their spasticity on a 0-to-10 numeric rating scale, in which 0 signifies no spasticity and 10 the worst possible spasticity.18 See Table 117-20 for a description of scales used in evaluat-ing spasticity, clonus, and muscle tightness.

Treatment. Spasticity is managed through vari-ous treatments based on specific patient needs. Cen-trally acting antispasmodic medications, such as baclofen and tizanidine (Zanaflex), are commonly used. Adverse effects of these medications include sedation, dizziness, gastrointestinal upset, hypoten-sion, headache, convulsions, agitation, leukocyto-sis, chills, urinary retention or frequency, hypotonia, and dry mouth. Patients who cannot tolerate adverse effects of large doses may require an intrathecal ba-clofen pump, which enables therapeutic management at lower doses with fewer adverse effects. Good candi-dates for this treatment are patients who have lower limb spasticity and are unable to tolerate oral baclofen or require higher doses to manage spasticity.21 Patients

Spinal cord

Corticospinal tract(upper motor neuron)

Interneuron

Primary motorcortex

Lower motorneuron

Skeletal muscle

Figure 2. The Upper Motor Neuronal Pathway

An upper motor neuron descends through the corticospinal tract and synapses in the gray matter of the spinal cord to a lower motor neuron, which innervates skeletal muscle. If present, the interneuron at the synapse can be excitatory or inhibitory. If the upper motor neuron is damaged, it can be either difficult to inhibit the muscle, resulting in spasticity, or difficult to excite the mus-cle, resulting in muscle weakness.

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who experience focal spasticity, however, can of-ten manage symptoms through botulinum toxin in-jections in upper or lower extremities. Botulinum toxin is a neuromuscular blocker and a muscle re-laxant. Another treatment option is the injection of the chemical neurolytic phenol directly into the pe-ripheral nerves to block the stimulus that activates overactive muscles in spasticity. In some severe cases, selective dorsal rhizotomy surgery, in which spasticity-causing nerve roots are isolated and destroyed, is per-formed.

Physical and occupational therapies are manage-ment strategies commonly used by patients with spas-ticity, who often struggle with mobility and activities of daily living. Nursing modalities for patients with spasticity include heat, stretching, massage, and aro-matherapy. Some research indicates that ice may be helpful as well.22 Ice, however, is not commonly used in clinical practice. Some patients have reported that

alternative therapies, such as acupuncture, are benefi-cial in treating spasticity.23, 24

CLONUSClonus is a neurologic symptom that manifests as an abnormal contracting and relaxing of the affected body part. Patients often experience clonus, spasticity, and neuropathic pain concurrently. Discrimination among these various symptoms may be difficult.25, 26 Clonus, however, has a distinct pattern in which the first oscillation (contraction and relaxation cycle) is longer than subsequent oscillations.27

Pathophysiology. Clonus is an involuntary, rhyth-mic response to stretch reflex stimulus. Though clonus is more often induced in the ankles and feet, it can oc-cur at the patella, triceps surface, wrist, jaw, and biceps brachii. For example, when the ankle is dorsiflexed, muscle spindles are stretched in the gastrocnemius and soleus muscles. Depolarization of the spindles

Scale Technique Rater(s) Scoring

Ashworth17 Resistance or catch when “quick” PROM is performed

Expert assessors

0 No increase

1 Slight increase in tone, giving a “catch” when limb is moved in flex-ion or extension

2 More marked increase in tone but limb is easily flexed

3 Considerable increase in tone—passive movement is difficult

4 Limb rigid in flexion or extension

Modified Ashworth18

Resistance or catch when “quick” PROM is performed

Expert assessors

0 No increase

1 Slight increase in muscle tone, manifested by a catch and release or by minimal resistance at the end of the ROM when limb is moved in flexion or extension

1+ Slight increase in muscle tone, manifested by a catch, followed by min-imal resistance throughout the remainder (less than half) of the ROM

2 More marked increase in muscle tone through most of the ROM, but limb is easily moved

3 Considerable increase in muscle tone, passive movement is difficult

4 Limb is rigid in flexion or extension

Numeric Rating Scale19, a

Patient self- report of spasticity

Patient(s) 010

No spasticityWorst possible spasticity

Spasm Frequency Score20

Frequency of clo-nus elicited with PROM or activity

Any clinician

0 No spasms

1 Mild spasms induced by stimulation

2 Infrequent full spasms occurring less than once per hour

3 Spasms occurring more than once per hour

4 Spasms occurring more than 10 times per hour

Table 1. Assessment Scales for Spasticity, Clonus, and Muscle Tightness

PROM = passive range of motion; ROM = range of motion.a Numeric rating scales can also be used to assess muscle tightness.

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generates action potentials, which are transmitted to the spinal cord by sensory neurons called Ia affer-ents. Ia afferents synapse on the α motor neurons to the calf, leading to increased activation of the gas-trocnemius and soleus.25 The foot vigorously points downward (plantar flexion) and then releases back into dorsiflexion, such that the gastrocnemius and soleus are stretched repeatedly as oscillating con-tractions move the foot from dorsiflexion to plantar flexion (see Figure 3). The first oscillation is always the longest, with subsequent oscillations becoming shorter and eventually stabilizing into a rhythmic pattern by the fourth or fifth repetition until the oscillations stop.27 As with spasticity, clonus results from increased excitability of the α motor neurons, brought on by impaired descending inhibitory path-ways. Highly activated γ motor neurons increase the sensitivity of muscle spindles, making the oscillating circuit possible.28

Assessment. Clonic oscillations are episodic. The frequency of oscillations can be visually assessed us-ing the Spasm Frequency Score proposed by Penn and colleagues in 1989 as a means of reporting the ef-fects of intrathecal baclofen for spinal spasticity.20 The Spasm Frequency Score can be used by both clinicians and patients to report the frequency (the number per hour) of clonic oscillations, which can increase if co-existing spasticity worsens.

Treatment. Clonus is managed medically with such oral medications as tizanidine, baclofen, diazepam

(Valium), clonazepam (Klonopin), and dantrolene (Dantrium). Diazepam and clonazepam are schedule IV anxiolytics, which can depress the central nervous system. Some researchers have reported that botuli-num toxin and phenol injections may be beneficial in treating clonus.29, 30 The application of cold packs27, 31 and manual pressure32, 33 are common nursing treat-ments for clonus.

DIFFERENTIATING MOVEMENT DISORDERSSpasticity, clonus, and muscle tightness may appear to be similar, but there are important differences be-tween them. Spasticity and clonus are neurogenic conditions resulting from a disruption in upper mo-tor neuronal pathways, while muscle tightness is an orthopedic condition that results from traumatic in-jury. While spasticity and clonus arise with neuro-logic injury, they are not progressive in nature. They may, however, be exacerbated by noxious stimuli or comorbid conditions. Muscle tightness, on the other hand, can progress if not managed appropriately in the initial phase of injury.34

There are differences and commonalities in the management of these conditions. All three can be managed through oral medications such as baclofen and tizanidine; however, use of botulinum toxin or the intrathecal baclofen pump is reserved for spastic-ity and in some cases clonus. Ice packs can be used to manage clonus and muscle tightness but is not pre-ferred for spasticity. Similarly, heat may help reduce

Dorsal �exion is the originalstimulus

Stretch ofgastrocnemius and soleus (calf)muscles

Stretch of musclespindles in the calfmuscle Increased action

potential frequencyin Ia sensory neuronsto the spinal cord

Activation of theα motor neuronsprojecting from thespinal cord to the calf

Vigorous contraction of thecalf muscles andplantar �exionof the foot

Relaxation of thecalf with completionof the stretch re�ex

Connective tissue element inlower leg returnsfoot to positionof dorsal �exion

After 4 to 5loops the re�exresponse is lessthan requiredfor reexcitation

Dorsal �exion of thefoot reexcites there�ex albeit slightlyless vigorously

Figure 3. The Feedback Loop Demonstrated in Clonus of the Foot

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spasticity and muscle tightness but not clonus. Man-ual pressure may help temporarily stop clonus, while stretching, repositioning, and massage may alleviate spasticity and muscle tightness.

Nurses working in a variety of settings are likely to encounter patients with symptoms of spasticity, clonus, and muscle tightness. To effectively manage these frequently overlapping disorders, nurses must understand the underlying pathophysiology of each. Future research should focus on identifying continu-ing education strategies that allow nurses to learn about these movement disorders and translate their knowledge into bedside evidence-based practice. ▼

Rozina Bhimani is an assistant professor in the School of Nursing at the University of Minnesota Twin Cities, Minneapolis, where Frank Medina is a research assistant in the College of Liberal Arts and Lisa Carney-Anderson is an assistant professor in the School of Medicine, Department of Integrative Biology and Physiology. Contact author: Rozina Bhimani, bhim0001@umn.edu. This arti-cle was supported by a grant presented to Dr. Bhimani from the Nursing Foundation, School of Nursing, University of Minnesota (No. 1701-11304-21296). The authors and planners have dis-closed no potential conflicts of interest, financial or otherwise.

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For six additional continuing nursing activities re-lated to movement disorders, go to www.nursing center.com/ce.

To see a short video on spasticity, go to www.youtube.com/watch?v=TFmSM7SoXDg. To see examples of clonus and how to test for it, go to www.youtube.com/watch?v=MUOwuxiI5Gw and www.youtube.com/watch?v=UX75k8s5QUE.